Evidence map›Paper›PMID 28253990›Full record

ReviewProgress in molecular biology and translational science2017

Mitochondrial Perturbation in Alzheimer's Disease and Diabetes.

F Akhter, D Chen, S F Yan, S S Yan

Open access · greenAbstract readReview
In one paragraph

Review in Progress in molecular biology and translational science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
10.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. The Azalea Hypothesis of Alzheimer Disease: A Functional Iron Deficiency Promotes Neurodegeneration.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024
    Review
  8. Review
  9. Review
  10. Review
  11. GlyNAC (Glycine andAntioxidants (Basel, Switzerland) · 2022
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

F AkhterSchool of Pharmacy, Higuchi Bioscience Center, University of Kansas, Lawrence, KS, United States.
D ChenSchool of Pharmacy, Higuchi Bioscience Center, University of Kansas, Lawrence, KS, United States.
S F YanSchool of Pharmacy, Higuchi Bioscience Center, University of Kansas, Lawrence, KS, United States.
S S YanSchool of Pharmacy, Higuchi Bioscience Center, University of Kansas, Lawrence, KS, United States. Electronic address: shidu@ku.edu.
University of Kansas · US

Funding

University of Kansas Alzheimer's Disease Core CentersP30AG035982 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI BROOKS, WILLIAM M. · 2011 to 2020
$16.6M
Role of Cyclophilin D in Abeta-induced synaptic injuryR37AG037319 · NIA · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHIRLEY SHIDU · 2010 to 2019
$3.1M
TOMM40-mediated mitochondrial dysfunction and Alzheimers diseaseR01AG053041 · NIA · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHIRLEY SHIDU · 2017 to 2021
$2.7M
Mitochondrial degrading enzyme, synaptic mitochondrial function in AD mouse modelR01AG044793 · NIA · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHIRLEY SHIDU · 2014 to 2018
$1.9M
RAGE and mitochondrial degeneration in diabetesR01NS089116 · NINDS · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHIRLEY SHIDU · 2015 to 2018
$1.5M
NIA NIH HHS P30 AG035982NIA NIH HHS R01 AG044793NIA NIH HHS R01 AG053041NIA NIH HHS R37 AG037319NINDS NIH HHS R01 NS089116
6 · The paper itself

Abstract

Mitochondria are well-known cellular organelles that play a vital role in cellular bioenergetics, heme biosynthesis, thermogenesis, calcium homeostasis, lipid catabolism, and other metabolic activities. Given the extensive role of mitochondria in cell function, mitochondrial dysfunction plays a part in many diseases, including diabetes and Alzheimer's disease (AD). In most cases, there is overwhelming evidence that impaired mitochondrial function is a causative factor in these diseases. Studying mitochondrial function in diseased cells vs healthy cells may reveal the modified mechanisms and molecular components involved in specific disease states. In this chapter, we provide a concise overview of the major recent findings on mitochondrial abnormalities and their link to synaptic dysfunction relevant to neurodegeneration and cognitive decline in AD and diabetes. Our increased understanding of the role of mitochondrial perturbation indicates that the development of specific small molecules targeting aberrant mitochondrial function could provide therapeutic benefits for the brain in combating aging-related dementia and neurodegenerative diseases by powering up brain energy and improving synaptic function and transmission.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsDiabetes MellitusHumansMitochondriaNeuronsSynapsesAmyloid beta-PeptidesAlzheimer diseaseDiabetesMitochondrial dysfunctionNeuronal toxicitySynaptic degeneration aging

Identifiers

PMID28253990
PMCPMC5896572
OpenAlexW2584358826

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.